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Published online before print May 17, 2007, 10.1097/PSY.0b013e318049cc2d
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Psychosomatic Medicine 69:356-364 (2007)
© 2007 American Psychosomatic Society


ORIGINAL ARTICLES

Bivariate Genetic Modeling of Cardiovascular Stress Reactivity: Does Stress Uncover Genetic Variance?

Eco J. C. De Geus, PhD, Nina Kupper, PhD, Dorret I. Boomsma, PhD and Harold Snieder, PhD

From the Department of Biological Psychology (E.J.C.D.G., N.K., D.I.B.), Vrije Universiteit Amsterdam, Netherlands; Department of Medical Psychology (N.K.), Tilburg University, Netherlands; Georgia Prevention Institute (H.S.), Department of Pediatrics, Medical College of Georgia, Augusta, Georgia; Twin Research and Genetic Epidemiology Unit (H.S.), St. Thomas’ Campus, King’s College, London, UK.

Address correspondence and reprint requests to Eco J. C. De Geus, Department of Biological Psychology, Vrije Universiteit, van der Boechorststraat 1, 1081 BT, Amsterdam, Netherlands. E-mail: eco{at}psy.vu.nl

Objective: To test the existence of gene-by-stress interaction by assessing cardiovascular stress reactivity in monozygotic and dizygotic twins.

Methods: We studied 160 adolescent (mean age 16.7 ± 2.0 years; range 13–22 years) and 212 middle-aged twin pairs (mean age 44.2 ± 6.7 years; range 34–63 years). Systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), pre-ejection period (PEP), and respiratory sinus arrhythmia (RSA) were measured at rest and during a choice reaction time and a mental arithmetic task. We used a bivariate analysis of the resting and mean stress levels to test for gene-by-stress interaction, which can be caused by the emergence of new genetic variance specific to stress or by stress-induced amplification of the existing genetic variance at rest.

Results: Genetic factors significantly contributed to individual differences in resting SBP, DBP, HR, PEP, and RSA levels in the adolescent (heritability range 0.31–0.70) and middle-aged (heritability range 0.32–0.64) cohorts. The effect of these genetic factors was amplified by stress for all variables in the adolescent cohort, and for SBP in the middle-aged cohort. In addition, stress-specific genetic variation emerged for HR in both cohorts and for PEP and SBP in the adolescent cohort. Heritability of stress levels of SBP, DBP, HR, PEP, and RSA ranged from 0.54 to 0.74 in the adolescents and from 0.44 to 0.64 in the middle-aged cohort.

Conclusions: Stress uncovers genetic variance in BP, HR, and cardiac sympathovagal balance through the emergence of new stress-specific genetic effects and the amplification of existing genetic effects that also affect the resting values.

Key Words: twin study • heritability • heart rate • blood pressure • pre-ejection period • respiratory sinus arrhythmia

Abbreviations: SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate; PEP = pre-ejection period; RSA = respiratory sinus arrhythmia; MZ = monozygotic; DZ = dizygotic; MZM = monozygotic males; MZF = monozygotic females; DZM = dizygotic males; DZF = dizygotic females; DOS = dizygotic twin pairs of opposite sex; h2 = heritability; LDL-C = low-density lipoprotein cholesterol; HDL-C = high-density lipoprotein cholesterol; BMI = body mass index; ECG = electrocardiogram; ICG = impedance cardiogram; PCG = phonocardiogram.




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